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. 2018 Jan 18;25(8):1457–1472. doi: 10.1038/s41418-017-0053-8

Fig. 2.

Fig. 2

miR-137 regulates the lipid metabolism of melanoma cells. a miR-137 overexpression significantly suppressed the erastin- and RSL3-induced lipid formation. Indicated cells were treated with erastin (5 µM in A375, 10 µM in G-361) or RSL3 (0.1 µM in A375, 0.5 µM in G-361) for 24 h. The lipid formation was measured by MDA assay. Data shown represent mean ± SD from three independent experiments. **p < 0.01. b miR-137 antagomirs significantly increased the erastin- and RSL3-induced lipid formation. Indicated cells were treated with erastin (5 µM in A375, 10 µM in G-361) or RSL3 (0.1 µM in A375, 0.5 µM in G-361) for 24 h. The lipid formation was measured by MDA assay. Data shown represent mean ± SD from three independent experiments. **p < 0.01. c Overexpression of miR-137 significantly suppressed erastin- and RSL3-induced lipid ROS level as assessed by flow cytometry using C11-BODIPY. Indicated cells were treated with erastin (5 µM in A375, 10 µM in G-361) or RSL3 (0.1 µM in A375, 0.5 µM in G-361) for 24 h. d Cells transfected with miR-137 antagomirs showed increased lipid ROS level as assessed by BODIPY-C11 staining. Indicated cells were treated with erastin (5 µM in A375, 10 µM in G-361) or RSL3 (0.1 µM in A375, 0.5 µM in G-361) for 24 h. e, f The expression levels of miR-137 influences the Fe2+ accumulation in erastin or RSL3-treated A375 and G-361 cells. Indicated cells were treated with erastin (5 µM in A375, 10 µM in G-361) or RSL3 (0.1 µM in A375, 0.5 µM in G-361) for 24 h and the intracellular Fe2+ was assayed. Data shown represent mean ± SD from three independent experiments. *p < 0.05